Parathyroid hormone regulates histone deacetylases in osteoblasts

Emi Shimizu, Nagarajan Selvamurugan, Jennifer J. Westendorf, Nicola C. Partridge

Research output: Chapter in Book/Report/Conference proceedingConference contribution

16 Scopus citations

Abstract

Parathyroid hormone (PTH) functions as an essential regulator of calcium homeostasis and as a mediator of bone remodeling. We have already shown that PTH stimulates the expression of matrix metalloproteinase-13 (MMP-13), which is responsible for degrading components of extracellular matrix. We have hypothesized that histone deacetylases (HDACs) are involved with PTH-induced MMP-13 gene expression in the osteoblastic cell line, UMR 106-01. We have shown that PTH profoundly regulates HDAC4 in UMR 106-01 cells through a PKA-dependent pathway, leading to removal of HDAC4 from the MMP-13 promoter and its enhanced transcription. Understanding the mechanism of how HDACs affect osteoblast differentiation and mineralization will identify new theraupeutic methods for bone diseases, such as osteoporosis and multiple myeloma.

Original languageEnglish (US)
Title of host publicationSkeletal Biology and Medicine, Part A
Subtitle of host publicationAspects of Bone Morphogenesis and Remodeling
PublisherBlackwell Publishing Inc.
Pages349-353
Number of pages5
ISBN (Print)9781573316842
DOIs
StatePublished - Nov 2007

Publication series

NameAnnals of the New York Academy of Sciences
Volume1116
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Histone deacetylases
  • Osteoblasts
  • Parathyroid hormone

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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  • Cite this

    Shimizu, E., Selvamurugan, N., Westendorf, J. J., & Partridge, N. C. (2007). Parathyroid hormone regulates histone deacetylases in osteoblasts. In Skeletal Biology and Medicine, Part A: Aspects of Bone Morphogenesis and Remodeling (pp. 349-353). (Annals of the New York Academy of Sciences; Vol. 1116). Blackwell Publishing Inc.. https://doi.org/10.1196/annals.1402.037